%0 Journal Article %1 Wier_1995_146 %A Wier, W. G. %A L�pez-L�pez, J. R. %A Shacklock, P. S. %A Balke, C. W. %D 1995 %J Ciba Found Symp %K 7587615 Animals, Calcium Calcium, Channel Channels, Confocal, Electric Gating, Gov't, Guinea In Ion Membrane Microscopy, Myocardium, Non-U.S., P.H.S., Patch-Clamp Pigs, Potentials, Probability, Research Reticulum, Sarcoplasmic Signal Stimulation, Support, Techniques, Transduction, U.S. Verapamil, Vitro, %P 146--60; discussion 160-4 %T Calcium signalling in cardiac muscle cells. %V 188 %X In heart cells, several distinct kinds of transient spatial patterns of cytoplasmic calcium ion concentration (Ca$^2+$i) can be observed: (1) Ca$^2+$i waves, in which regions of spontaneously increased Ca$^2+$i propagate at high velocity (100 microns/s) through the cell; (2) Ca$^2+$ 'sparks', which are spontaneous, non-propagating changes in Ca$^2+$i that are localized in small (approximately 2 microns) subcellular regions; and (3) evoked Ca$^2+$i transients that are elicited by electrical depolarization, in association with normal excitation-contraction (E-C) coupling. In confocal Ca$^2+$i images, evoked Ca$^2+$i transients appear to be nearly spatially uniform throughout the cell, except during their rising phase or during small depolarizations. In contrast to Ca$^2+$i waves and spontaneous Ca$^2+$ sparks, evoked Ca$^2+$i transients are triggered by L-type Ca$^2+$ channel current and they are 'controlled', in the sense that stopping the L-type Ca$^2+$ current stops them. Despite their different characteristics, all three types of Ca$^2+$ transient involve Ca$^2+$-induced release of Ca$^2+$ from the sarcoplasmic reticulum. Here, we address the question of how the autocatalytic process of Ca$^2+$-induced Ca$^2+$ release, which can easily be understood to underlie spontaneous regenerative ('uncontrolled'), propagating Ca$^2+$i waves, might be 'harnessed', under other circumstances, to produce controlled changes in Ca$^2+$i, as during normal excitation-contraction coupling, or changes in Ca$^2+$i that do not propagate. We discuss our observations of Ca$^2+$ waves, Ca$^2+$ sparks and normal Ca$^2+$ transients in heart cells and review our results on the 'gain' of Ca$^2+$-induced Ca$^2+$ release. We discuss a model involving Ca$^2+$ microdomains beneath L-type Ca$^2+$ channels, and clusters of Ca$^2+$-activated Ca$^2+$ release channels in the sarcoplasmic reticulum which may form the basis of the answer to this question.

@article{Wier_1995_146, abstract = {In heart cells, several distinct kinds of transient spatial patterns of cytoplasmic calcium ion concentration ([{C}a$^{2+}$]i) can be observed: (1) [{C}a$^{2+}$]i waves, in which regions of spontaneously increased [{C}a$^{2+}$]i propagate at high velocity (100 microns/s) through the cell; (2) {C}a$^{2+}$ 'sparks', which are spontaneous, non-propagating changes in [{C}a$^{2+}$]i that are localized in small (approximately 2 microns) subcellular regions; and (3) evoked [{C}a$^{2+}$]i transients that are elicited by electrical depolarization, in association with normal excitation-contraction (E-C) coupling. In confocal [{C}a$^{2+}$]i images, evoked [{C}a$^{2+}$]i transients appear to be nearly spatially uniform throughout the cell, except during their rising phase or during small depolarizations. In contrast to [{C}a$^{2+}$]i waves and spontaneous {C}a$^{2+}$ sparks, evoked [{C}a$^{2+}$]i transients are triggered by L-type {C}a$^{2+}$ channel current and they are 'controlled', in the sense that stopping the L-type {C}a$^{2+}$ current stops them. Despite their different characteristics, all three types of {C}a$^{2+}$ transient involve {C}a$^{2+}$-induced release of {C}a$^{2+}$ from the sarcoplasmic reticulum. Here, we address the question of how the autocatalytic process of {C}a$^{2+}$-induced {C}a$^{2+}$ release, which can easily be understood to underlie spontaneous regenerative ('uncontrolled'), propagating [{C}a$^{2+}$]i waves, might be 'harnessed', under other circumstances, to produce controlled changes in [{C}a$^{2+}$]i, as during normal excitation-contraction coupling, or changes in [{C}a$^{2+}$]i that do not propagate. We discuss our observations of {C}a$^{2+}$ waves, {C}a$^{2+}$ sparks and normal {C}a$^{2+}$ transients in heart cells and review our results on the 'gain' of {C}a$^{2+}$-induced {C}a$^{2+}$ release. We discuss a model involving {C}a$^{2+}$ microdomains beneath L-type {C}a$^{2+}$ channels, and clusters of {C}a$^{2+}$-activated {C}a$^{2+}$ release channels in the sarcoplasmic reticulum which may form the basis of the answer to this question.}, added-at = {2009-06-03T11:20:58.000+0200}, author = {Wier, W. G. and L�pez-L�pez, J. R. and Shacklock, P. S. and Balke, C. W.}, biburl = {https://www.bibsonomy.org/bibtex/207a88ccefc1037fca5ae5090ed3dd661/hake}, description = {The whole bibliography file I use.}, interhash = {76e5b67313a1dab72d46193f747e8f85}, intrahash = {07a88ccefc1037fca5ae5090ed3dd661}, journal = {Ciba Found Symp}, keywords = {7587615 Animals, Calcium Calcium, Channel Channels, Confocal, Electric Gating, Gov't, Guinea In Ion Membrane Microscopy, Myocardium, Non-U.S., P.H.S., Patch-Clamp Pigs, Potentials, Probability, Research Reticulum, Sarcoplasmic Signal Stimulation, Support, Techniques, Transduction, U.S. Verapamil, Vitro,}, pages = {146--60; discussion 160-4}, pmid = {7587615}, timestamp = {2009-06-03T11:21:37.000+0200}, title = {Calcium signalling in cardiac muscle cells.}, volume = 188, year = 1995 }